title: U-waves and T-wave peak to T-wave end intervals in patients with catecholaminergic polymorphic ventricular tachycardia, effects of beta-blockers.
abstract: BACKGROUND
  Catecholaminergic polymorphic ventricular tachycardia (CPVT) is characterized by risk of polymorphic ventricular tachycardia (pVT) and sudden death during stress. Experimental CPVT models show that delayed afterdepolarization (DAD)-induced triggered activity is the initiating mechanism of pVT, whereas an increase in transmural dispersion of repolarization (TDR) controls degeneration of pVT to ventricular fibrillation. U-wave and T-wave peak to T-wave end interval (TPE) are regarded as electrocardiographic counterparts of DAD and TDR, respectively.
  
  
  OBJECTIVE
  We tested hypotheses that patients with CPVT might show abnormal U-waves and TPE intervals and that beta-blockers could suppress appearance of these repolarization abnormalities.
  
  
  METHODS
  We reviewed Holter recordings from 19 CPVT patients with a RyR2 mutation (P2328S or V4653F) and from 19 healthy unaffected subjects to record U-waves and TPE intervals as well as to measure beta-blockers' effects on ventricular repolarization by use of an automated computerized program.
  
  
  RESULTS
  The maximal U-wave to T-wave amplitude ratio was 0.8 +/- 0.6 in CPVT patients and 0.4 +/- 0.3 in unaffected subjects (P = .009). Patients with most ventricular extrasystoles had a higher U-wave to T-wave amplitude ratio than those with fewest extrasystoles. Treatment with beta-blockers decreased U-wave amplitude at high heart rates. CPVT patients had longer TPE intervals than unaffected subjects at high heart rates, and beta-blocker treatment shortened their TPE intervals.
  
  
  CONCLUSIONS
  Present data support the hypothesis that U-waves associate with the DAD-triggered extrasystolic activity in CPVT patients. Patients with a RyR2 mutation show increased TPE at high heart rates. Beta-blocker treatment suppresses observed repolarization abnormalities in CPVT patients.
authors.affiliation: Department of Cardiology, Helsinki University Central Hospital, Helsinki, Finland. matti.viitasalo@hus.fi.
authors.forename: Matti
authors.initials: M
authors.lastname: Viitasalo
authors.forename: Lasse
authors.initials: L
authors.lastname: Oikarinen
authors.forename: Heikki
authors.initials: H
authors.lastname: Väänänen
authors.forename: Kimmo
authors.initials: K
authors.lastname: Kontula
authors.forename: Lauri
authors.initials: L
authors.lastname: Toivonen
authors.forename: Heikki
authors.initials: H
authors.lastname: Swan
mesh_terms: D000293:Adolescent; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology* / Q000627:therapeutic use*; D000328:Adult; D015716:Electrocardiography, Ambulatory; D005260:Female; D006339:Heart Rate; D006801:Humans; D008297:Male; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism*; D017180:Tachycardia, Ventricular / Q000188:drug therapy* / Q000235:genetics*
chemical_list: D000319:Adrenergic beta-Antagonists; D019837:Ryanodine Receptor Calcium Release Channel